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Fall 1997 Newsletter

Bovine Respiratory
(Footrot) of Cattle
PCR for the
Detection of Lawsoniain-
tracellularis, Serpulinahyo-

and salmonellaspp.
from Porcine Intestinal Specimens
Enteric Canine
Parvovirus Infection
Plant Toxicities
Diseases of
Yew Poisoning
in Livestock
Serum Vitamin E Analysis


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Polioencephalomalacia is a thiamine-responsive disease of ruminants. It was first described as thiaminedeficiency, however, more recent evidence indicates that the disease actually results from a disturbance in thiamine metabolism.   Proposed mech­anisms include increased numbers of thiaminase producing bacteria in the rumen, production or ingestion of thiamine analogs, ingestion of thiaminases (as in bracken fem), impaired thiamine absorption, and increased excretion of thiamine. Animals on high-concentrate diets are at greater risk of developing the disease, presumably because the low rumen pH decreases the numbers of thiamine-producing bacteria and increases the numbers of thiaminase producing bacteria.   High sulfur diets, amprolium, thiobendazole and levamisolehydrochloride use have also been associated with this disorder. Clinical signs of polioencephalo-malacia range from dullness, head pressing and blindness to opisthotonus, muscle tremors, twitching, hypersalivation, coma and death.  Antemortem  confirmation of a diagnosis  of Polioencephalomalacia  is difficult.    The best indicator may be measurement of the thiamine-dependent enzyme, erythrocytetransketolase. Levels of this enzyme are a relatively sensitive and specific indicator of active thiamine levels. The test compares the levels of the active enzyme to its inactive form. In animals with Polioencephalomalacia, the levels of the inactive enzyme are increased.   Rumen content analysis that shows a decrease in gram-positive cocci and coccobacilli and an increase in gram-positive bacilli is also indicative of deranged thiamine metabolism. Looking for decreased thiamine pyro-phospate levels in erythrocytes or rumen fluid may be useful. However, decreases are not always seen in polioencephalomalaciaand therefore, these tests are unreliable. Thiaminase may be measured in the rumen and feces of affected animals,

Gross lesions of polioencephalo­malacia include swelling of the cerebrum, evidenced by flattened gyri and shallow sulci. The cerebral cortex may be thinned. The distribution is symmetrical.  On cut section, a pale layer may be visible near the junction of the gray and white matter. The affected areas of cortex will fluoresce under UV light.

Histological lesions include laminar necrosis of cerebral neuronal cell bodies. The deeper layers are more severely affected. The neurons appear shrunken and eosinophilic, and are surrounded by a clear space. Spongiosis is evident in the cortex and the white matter immediately adjacent to the cortex. Vessels in the meninges are often congested with small to moderate accumulations of leukocytes. If the animal survives over a week, liquefactive necrosis is evident in the affected areas. The necrotic tissue is eventually removed by phagocytes.

Differential diagnoses that should be considered for the clinical signs of polio- encephalomalacia include rabies, lead or other heavy metal poisoning, vitamin A deficiency, ethyleneglycol intoxication, EBR encephalitis (in young calves), and salt poisoning. If a presumptive diagnosis of polioencephalomalacia can be made based on history, treatment should be initiated to prevent further cerebral necrosis.

If diagnosed and treated early in the course of the disease, affected animals may recover   completely   with   treatment. Thiamine (10-20 mg/kg) is administered intramuscularly or subcutaneously three times a day. If it is necessary to administer the initial treatment intravenously, it must be diluted in an isotonic fluid and administered slowly.  Some animals may require con­current therapy for convulsions. Improve­ment is usually evident within 24 hours of treatment,  however,   severely  affected animals may require up to one week to recover. Blindness may be permanent in these animals.

Polioencephalomalacia   may   be prevented by supplementing thiamine in the ration. Ruminants should be adapted slowly to new diets. Cobalt supplementation may be necessary in deficient areas. Calcium sulfate supplement, high-sulfur sources of water, such as well-water, should be avoided in the diet.

- byDianeFeutz Norton, Class of 1998

- edited by Lydia Andrews-Jones, DVM


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